Hypercapnic acidosis decreases the rate of glucose utilization by rat brain and endogenous intermediary metabolites and amino acids are oxidized to maintain normal oxygen consumption. Our studies examine those phenomena in developing rat brain. The rate of brain glucose utilization is measured by a method based on the 'trapping' in intermediary metabolites and amino acids of C14 derived from blood (2-C14)-glucose. Intermediary metabolites and amino acids are assayed enzymatically. We will test the hypothesis that proteins are degraded during prolonged hypercapnia to supply amino acids for oxidation. The mechanism of the decrease in glucose utilization will be studied to identify the primary events (e.g. inhibition of phosphofructokinase) and the 'active' agent (the increase in H ion or CO2). This work is intended to provide the basis for future studies relating temporary alterations in brain intermediary metabolism during development to long term changes in brain function. BIBLIOGRAPHIC REFERENCE: Miller, A.L., Hawkins, R.A. and Veech, R.L. "Decreased Rate of Glucose Utilization by Rat Brain in vivo after Exposure to Atmospheres Containing High Concentrations of CO2". J. Neurochem. 25, 553-558 (1975).